Vasomotor neurons

Sun M-K, Reis DJ. Hypoxia selectively excites vasomotor neurons of rostral ventrolateral medulla in rats. Am J Physiol 1994 266 R245-R256. 

Following ehemodenervation in the anesthetized animal, systemic hypoxia produces a powerful increase in sympathetic discharge and arterial blood pressure (61-63). That this is mediated in the brainstem is indicated by a similar effect of the injeetion of hypoxie saline or cyanide (NaCN) in the right vertebral artery of the anesthetized deafferented cat (64). This response has been shown to be mediated by reticulospinal vasomotor neurons located in the RVLM (63,65,66) that appear to be essential for the generation and reflex regulations of arterial blood pressure (67). 

There is substantial evidence fi om studies in the intact animal that these neurons are directly stimulated by hypoxia. Sun and colleagues have shown that microinjection of cyanide into the RVLM of rats evokes a pressor response (68). The RVLM reticulospinal sympathoexcitatory vasomotor neurons, many of which exhibit pacemaker-hke activity, are rapidly and reversibly excited in a dose-dependent manner when the cyanide is delivered by either microinjection or microiontophoresis (63,66,68,69). This excitation is not altered by blockade of ionotropic excitatory amino acid (EAA) receptors in this region (70). Fiuiher, during hypoxic excitation of these RVLM reticulospinal sympathoexcitatory vasomotor neurons, their response to baroreceptor stimulation is preserved, suggesting that the... 

Ramirez et al. (82) produced bilateral synaptic blockade within the pre-BotC in pentobarbitone-anesthetized cats by injection of TTX and abolished eupneic ouQ)ut without eliminating the gasping response to severe hypoxia or asphyxia. It is important to note in this regard that Sun and Reis have shown that hypoxic excitation of reticulospinal sympathoexcitatory vasomotor neurons seems to be independent of synaptic transmission, or, at least, TTX-sensitive mechanisms (63,69,70 described above). If similar mechanisms exist in the pre-BotC, the inability of TTX to block hypoxia-induced gasping is not unexpected. 

Sun MK, Spyer KM. Responses of rostroventrolateral medulla spinal vasomotor neurones to chemoreceptor stimulation in rats. J Auton Nerv Syst 1991 33 79-84. 

Sun MK, Reis DJ. Hypoxic excitation of medullary vasomotor neurons in rats are not mediated by glutamate or nitric oxide. Neurosci Lett 1993 157 219-222. 

The mechanism of action of these drugs is caused by stimulation of o -adrenoreceptors in the inhibitory structure of the brain. It is believed that interaction of these drugs with adrenergic receptors is expressed in the suppression of vasomotor center neurons of the medulla, and reduction of hypothalamus activity, which leads to a decline in sympathetic impulses to the vessels and the heart. In summary, cardiac output and heart rate are moderately reduced, and consequently arterial pressure is reduced. 

The activation a2-adrenoceptors is particularly important in the negative feedback control of adrenergic outflow, centrally in the vasomotor centers and peripherally at the presynaptic axonal membrane of adrenergic neurons. 

These agents reduce sympathetic outflow from vasomotor centers in the brain stem but allow these centers to retain or even increase their sensitivity to baroreceptor control. Accordingly, the anti hypertensive and toxic actions of these drugs are generally less dependent on posture than are the effects of drugs that act directly on peripheral sympathetic neurons. 

Methyldopa and clonidine produce slightly different hemodynamic effects clonidine lowers heart rate and cardiac output more than does methyldopa. This difference suggests that these two drugs do not have identical sites of action. They may act primarily on different populations of neurons in the vasomotor centers of the brain stem. 

Stjame, P., Lundblad, L., Lundberg, J.M., Anggard, A. Capsaicin and nicotine-sensitive afferent neurones and nasal secretion in healthy human volunteers and in patients with vasomotor rhinitis, Br. J. Pharmacol. 1989, 96, 693-701. 

Tizanidine (Zanaflex) Tizanidine is used primarily for treating spasticity.14,24 This drug is similar to clonidine, but has less vasomotor effects and is therefore less likely to cause hypotension and other cardiovascular problems. As indicated earlier, tizanidine stimulates alpha-2 receptors in the spinal cord, which results in decreased excitatory input onto the alpha motor neuron. Decreased excitation of the alpha motor neuron results in decreased spasticity of the skeletal muscle supplied by that neuron. 

Tachykinins Neurons localized in the submucous and myenteric plexuses enterochromaffin cells in gut epithelium 1. Regulates vasomotor and gastrointestinal smooth muscle contraction 2. Mucus secretion and water absorption Direct and indirect activation of neurons in submucosa and myenteric plexuses in gut epithelium... 

Cell bodies of noradrenergic neurons located in the pons and brain stem project to all levels of the CNS. Agents that activate presynaptic alpha2 receptors on such neurons (eg, clonidine, methyldopa) decrease central noradrenergic activity, an action thought to result in decreased vasomotor outflow. Glutamate and substance P are not amines. The answer is (D). 

Studies in dogs have shown that PGEi may have a selective action on a group of neurones within the brain stem, the effect of which is to inhibit the irradiation of activity from respiratory to cardio-inhibitory and vasomotor pathways [437]. 

Ross CA, Ruggiero PA, Park DH, Joh TH, Sved AF, Femandez-Pardal J, Saacerdra JM, Reis DJ. Tonic vasomotor control by the rostral ventrolateral medulla effect of electrical or chemical stimulation of the area containing Cl adrenaline neurons on arterial pressure, heart rate, and plasma catecholamines and vasopressin. J Neurosci 1984 4 474-494. 

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